Kenny, P.J., Chen, S.A., Kitamura, O., Markou, A. Neurobiological evidence for hedonic allostasis associated with escalating cocaine use. Persistent obesity in rats following a period of consumption of a mixed, high energy diet. Construct validity of a self-stimulation threshold paradigm: effects of reward and performance manipulations.
Hedonic dysfunction manual#
Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) (American Psychiatric Association Publishing, Washington, D.C., 1994). Weight stigmatization and bias reduction: perspectives of overweight and obese adults. Puhl, R.M., Moss-Racusin, C.A., Schwartz, M.B. Perceptions of adolescents on overweight and obesity: the weight of opinion study. The role of dopamine in motivation for food in humans: implications for obesity. Addiction and its reward process through polymorphisms of the D2 dopamine receptor gene: a review. Relation between obesity and blunted striatal response to food is moderated by TaqIA A1 allele. Leptin regulates striatal regions and human eating behavior. The need to feed: homeostatic and hedonic control of eating. Common hedonic mechanisms may therefore underlie obesity and drug addiction. These data demonstrate that overconsumption of palatable food triggers addiction-like neuroadaptive responses in brain reward circuits and drives the development of compulsive eating. Moreover, lentivirus-mediated knockdown of striatal D2Rs rapidly accelerated the development of addiction-like reward deficits and the onset of compulsive-like food seeking in rats with extended access to palatable high-fat food. Striatal dopamine D2 receptors (D2Rs) were downregulated in obese rats, as has been reported in humans addicted to drugs. Accordingly, we detected compulsive-like feeding behavior in obese but not lean rats, measured as palatable food consumption that was resistant to disruption by an aversive conditioned stimulus. Similar changes in reward homeostasis induced by cocaine or heroin are considered to be crucial in triggering the transition from casual to compulsive drug-taking. We found that development of obesity was coupled with emergence of a progressively worsening deficit in neural reward responses.
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